按照血管紧张素转换酶(ACE)基因插入/缺失多态性不同，将92例2型糖尿病肾病患者分为II型组31例，ID型组30例及DD型组31例。用苯那普利治疗6个月后，观察治疗前后各组的尿白蛋白排泄率(UAER)、平均动脉压(MABP)、肌酐清除率(Ccr)及ACE的变化。结果：苯那普利治疗后3组UAER、MABP、ACE均下降，以II型组下降幅度最大(分别为58.6%、2.87kPa和72.3%)，DD型组下降幅度最小(P＜0.05)；而Ccr在DD型组下降幅度最大，II型组下降幅度最小(P＜0.05)；多元线性逐步回归分析显示：ACE基因型对UAER下降率有显著回归效果(R2=0.72，P＜0.001)。提示：ACE基因型影响血管紧张素转换酶抑制剂(ACEI)对糖尿病肾病的疗效，II基因型患者对ACEI治疗更为敏感。%The punpose of the researc h is to test the potential role of aninsertion/deletion polymorphism of angiotensin converting enzyme(ACE) gen e on the renoprotective responsiveness to benazepril in type 2 diabetes mellitus with nephropathy. Ninety-two cases with diabetes nephropathy were classified a ccording to the genotype of the ACE gene into three groups:31 cases with II geno types, 30 with ID and 31 with DD. Mean arterial blood pressure(MABP), urinary al buminexcretion rate(UAER), creatinine clearance rate(Ccr) and ACE levels were me asured before and after the six month treatment of benazepril(no differences in drug dose between the groups).Initiation of the 6-month treatment with bena zepril induced a signif icant drop in MABP, UAER and ACE levels in all three groups(P＜0.05), but th e reduction was significantly greater in patients with II genotype (UAER 58.6%, MABP 2.87 kPa, ACE 72.3%), compared with patients with either ID or DD geno type (P＜0.01, respectivly). A mild decline in the creatinine clearance rate was seen in all groups after the initiation of benazepril, but the change was highes t in DD group and lowest(P＜0.05) in II group . A multiple linear regression analysis revealed that the ACE gene polymorphism influenced the decline in albu minuria after initiation of ACE inhibition(R2=0.72, P＜0.001). The pa tients with II genotype are particularly susceptible to commonly advoca ted renoprotective treatment.
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